HORMONES, LYMPHOHEMATOPOIETIC CYTOKINES AND THE NEUROIMMUNE AXIS

The classical distinction between hormones and cytokines has become in creasingly obscure with the realization that homeostatic responses to infection involve coordinated changes in both the neuroendocrine and i mmune systems. The hypothesis that these systems communicate with one another is supported by the ever-accruing demonstrations of a shared m olecular network of ligands and receptors. For instance, leukocytes ex press receptors for hormones and these receptors modulate diverse biol ogical activities such as the growth, differentiation and effector fun ctions. Leukocyte lineages also synthesize and secrete hormones, such as insulin-like growth factor-I (IGF-I), in response to both growth ho rmone (GH) and also to cytokines such as tumor necrosis factor-alpha ( TNF-alpha). Since hormones share intracellular signaling substrates an d biological activities with classical lymphohemopoietic cytokines, ne uroendocrine and immune tissues share a common molecular language. The physiological significance of this shared molecular framework is that these homeostatic systems can intercommunicate. One important example of this interaction is the mechanism by which bacterial lipopolysacch aride, by eliciting a pro-inflammatory cytokine cascade from activated leukocytes, modulate pituitary GH secretion as well as other CNS-cont rolled behavioral and metabolic events. This article reviews the cellu lar and molecular basis for this communication system and proposes nov el mechanisms by which neuroendocrine-immune interactions converge to modulate disease resistance, metabolism and growth. Copyright (C) 1997 Elsevier Science Inc.